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虹鳟鱼红细胞暴露于病毒性出血性败血症病毒后，上调抗原加工机制和 MHC I&II、CD86 和 CD83 抗原呈递细胞标志物。

Rainbow Trout Red Blood Cells Exposed to Viral Hemorrhagic Septicemia Virus Up-Regulate Antigen-Processing Mechanisms and MHC I&II, CD86, and CD83 Antigen-presenting Cell Markers.

机构信息

Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE) and Instituto de Biología Molecular y Celular (IBMC), Universidad Miguel Hernández (UMH), 03202 Elche, Spain.

Instituto de Biología, Pontificia Universidad Católica de Valparaiso, 2373223 Valparaiso, Chile.

出版信息

Cells. 2019 Apr 27;8(5):386. doi: 10.3390/cells8050386.

DOI:10.3390/cells8050386
PMID:31035565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6562805/
Abstract

Nucleated teleost red blood cells (RBCs) are known to express molecules from the major histocompatibility complex and peptide-generating processes such as autophagy and proteasomes, but the role of RBCs in antigen presentation of viruses have not been studied yet. In this study, RBCs exposed ex vivo to viral hemorrhagic septicemia virus (VHSV) were evaluated by means of transcriptomic and proteomic approaches. Genes and proteins related to antigen presentation molecules, proteasome degradation, and autophagy were up-regulated. VHSV induced accumulation of ubiquitinated proteins in ex vivo VHSV-exposed RBCs and showed at the same time a decrease of proteasome activity. Furthermore, induction of autophagy was detected by evaluating LC3 protein levels. Sequestosome-1/p62 underwent degradation early after VHSV exposure, and it may be a link between ubiquitination and autophagy activation. Inhibition of autophagosome degradation with niclosamide resulted in intracellular detection of N protein of VHSV (NVHSV) and p62 accumulation. In addition, antigen presentation cell markers, such as major histocompatibility complex (MHC) class I & II, CD83, and CD86, increased at the transcriptional and translational level in rainbow trout RBCs exposed to VHSV. In summary, we show that nucleated rainbow trout RBCs can degrade VHSV while displaying an antigen-presenting cell (APC)-like profile.

摘要

已分化的硬骨鱼类红细胞（RBC）已知表达主要组织相容性复合体分子和肽生成过程相关分子，如自噬和蛋白酶体，但 RBC 在病毒抗原呈递中的作用尚未被研究。在这项研究中，通过转录组学和蛋白质组学方法评估了体外暴露于病毒性出血性败血症病毒（VHSV）的 RBC。与抗原呈递分子、蛋白酶体降解和自噬相关的基因和蛋白被上调。VHSV 诱导体外 VHSV 暴露 RBC 中泛素化蛋白的积累，并同时显示蛋白酶体活性降低。此外，通过评估 LC3 蛋白水平检测到自噬的诱导。VHSV 暴露后早期，自噬体降解的衔接蛋白-1/ p62 发生降解，它可能是泛素化和自噬激活之间的联系。用尼克酰胺抑制自噬体降解导致细胞内检测到 VHSV 的 N 蛋白（NVHSV）和 p62 积累。此外，在暴露于 VHSV 的虹鳟 RBC 中，主要组织相容性复合体（MHC）I 类和 II 类、CD83 和 CD86 等抗原呈递细胞标志物在转录和翻译水平上增加。总之，我们表明有核虹鳟 RBC 可以在降解 VHSV 的同时表现出抗原呈递细胞（APC）样特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/c3a22ee7daba/cells-08-00386-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/42fccf246f72/cells-08-00386-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/f2abb2ecdef3/cells-08-00386-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/4f7af4e22a42/cells-08-00386-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/c02ae4cb1b11/cells-08-00386-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/c3a22ee7daba/cells-08-00386-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/42fccf246f72/cells-08-00386-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/6b13bd7fc94d/cells-08-00386-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/9a1aa172b68a/cells-08-00386-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/183037a7cb4d/cells-08-00386-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/cb63c81ba94f/cells-08-00386-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/f2abb2ecdef3/cells-08-00386-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/4f7af4e22a42/cells-08-00386-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/c02ae4cb1b11/cells-08-00386-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d72/6562805/c3a22ee7daba/cells-08-00386-g009.jpg

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